SLU-PP-332
The Metabolic Accelerator
Exercise in a pill
The Metabolic Accelerator
Exercise in a pill
Be aware that during development compounds targeting nuclear receptors can have unpredictable effects. Only proceed with this thread if you are aware that no human safety data exists. (for the youngcels out there)
SLUPP332 is one of the most best attempts at exercise mimesis yet developed. This will cover the mechanisms, the actual risks.
my goal here is to elevate your uncertainty, wether you wanted to :
RUN IT or NOT
general info:
research date: 2023
Databases: PubMed/MEDLINE, Google Scholar, ClinicalTrials.gov
PRISMA summary: 23 records screened, 6 primary preclinical papers included, Human RCTs: 0
SLUPP332 is one of the most best attempts at exercise mimesis yet developed. This will cover the mechanisms, the actual risks.
my goal here is to elevate your uncertainty, wether you wanted to :
RUN IT or NOT
general info:
research date: 2023
Databases: PubMed/MEDLINE, Google Scholar, ClinicalTrials.gov
PRISMA summary: 23 records screened, 6 primary preclinical papers included, Human RCTs: 0
There is a lot of BS out there when it comes to metabolic enhancers, be it "no need to exercise, im a fat fuck"
Keep in mind SLUPP332 is not a stimulant. It does not work through adrenaline or dopamine. It works through transcriptional activation, which means onset is slow, effects are sustained, and cessation does not cause immediate crash.
Prolonged mitochondrial upregulation without compensatory adaptation is linked to (theoretical risks) oxidative stress and cardiac remodeling. This is not a fat burner This is a receptor agonist
Keep in mind SLUPP332 is not a stimulant. It does not work through adrenaline or dopamine. It works through transcriptional activation, which means onset is slow, effects are sustained, and cessation does not cause immediate crash.
Prolonged mitochondrial upregulation without compensatory adaptation is linked to (theoretical risks) oxidative stress and cardiac remodeling. This is not a fat burner This is a receptor agonist
The Estrogen related Receptor alpha and gamma (ERRαγ) both are the primary mediators of mitochondrial biogenesis and oxidative metabolism. They are part of the nuclear receptor superfamily but do not bind estrogen. Instead, they regulate energy metabolism genes in response to physiological stress.
We can directly modify the bodys oxidative capacity by influencing the ligands of ERRαγ. The primary endogenous coactivator is PGC 1α. SLUP s a synthetic agonist that upregulates this pathway directly.
Steroid users and the general population experience metabolic stagnation primarily because of mitochondrial downregulation, sedentary (cuck) behavior, and caloric excess. SLUP bypasses the signaling requirement and forces the transcriptional program.
Insulin resistance also causes metabolic inflexibility by suppressing oxidative pathways and upregulating lipogenesis. SLUP counteracts this by upregulating fatty acid oxidation genes.
There are plenty of other compounds that target metabolism including GW501516, SR9009, and DNP. Fortunately, SLUP operates through a mechanism with higher tissue specificity and potentially better safety margins, though this remains speculative and theoretical, you can always be the lab rat to my home bunker.
We can directly modify the bodys oxidative capacity by influencing the ligands of ERRαγ. The primary endogenous coactivator is PGC 1α. SLUP s a synthetic agonist that upregulates this pathway directly.
Steroid users and the general population experience metabolic stagnation primarily because of mitochondrial downregulation, sedentary (cuck) behavior, and caloric excess. SLUP bypasses the signaling requirement and forces the transcriptional program.
Insulin resistance also causes metabolic inflexibility by suppressing oxidative pathways and upregulating lipogenesis. SLUP counteracts this by upregulating fatty acid oxidation genes.
There are plenty of other compounds that target metabolism including GW501516, SR9009, and DNP. Fortunately, SLUP operates through a mechanism with higher tissue specificity and potentially better safety margins, though this remains speculative and theoretical, you can always be the lab rat to my home bunker.
The great thing about modifying the ERR pathway directly is that it is the holy grail for negating metabolic stagnation from most of the lifestyle failures you accumulate in your looksmaxxing journey.
Molecular Level:
SLUP binds ERRα/γ and upregulates recruitment of coactivator PGC-1α
(PPARGC1A) upregulates transcription of mitochondrial genes:
1)CPT1B (fatty acid transport)
2)MCAD/LCAD (β-oxidation)
3)ETC complexes I-V
4)TCA cycle enzymes
major effect : oxidative metabolism amplification
Cellular part
In skeletal muscle:
1)upregulation of mitochondrial density
2)upregulation of oxygen consumption rate
3)Shift toward oxidative Type 1 fiber pheno
4)upregulation of fatty acid oxidation
5)downregulation of glycolytic reliance
In adipose parts:
1)Possible upregulation of lipolysis
2)upregulation of energy dissipation
Systemic part:
in mice:
1)upregulation of energy expenditure
2)downregulation of adiposity
3)upregulation of insulin sensitivity
4)upregulation of treadmill endurance
Other ERR agonists like GSK4716 exist but have poor bioavailability. SLUP was structurally optimized for oral activity and receptor selectivity, making it the best characterized option in this class.
in secondary pathway interactions there are potential AMPK activation secondary to altered ATP/AMP ratio, crosstalk with thyroid hormone receptor pathways, and potential ROS increase due to higher mitochondrial flux.
Molecular Level:
SLUP binds ERRα/γ and upregulates recruitment of coactivator PGC-1α
(PPARGC1A) upregulates transcription of mitochondrial genes:
1)CPT1B (fatty acid transport)
2)MCAD/LCAD (β-oxidation)
3)ETC complexes I-V
4)TCA cycle enzymes
major effect : oxidative metabolism amplification
Cellular part
In skeletal muscle:
1)upregulation of mitochondrial density
2)upregulation of oxygen consumption rate
3)Shift toward oxidative Type 1 fiber pheno
4)upregulation of fatty acid oxidation
5)downregulation of glycolytic reliance
In adipose parts:
1)Possible upregulation of lipolysis
2)upregulation of energy dissipation
Systemic part:
in mice:
1)upregulation of energy expenditure
2)downregulation of adiposity
3)upregulation of insulin sensitivity
4)upregulation of treadmill endurance
Other ERR agonists like GSK4716 exist but have poor bioavailability. SLUP was structurally optimized for oral activity and receptor selectivity, making it the best characterized option in this class.
in secondary pathway interactions there are potential AMPK activation secondary to altered ATP/AMP ratio, crosstalk with thyroid hormone receptor pathways, and potential ROS increase due to higher mitochondrial flux.
Now for the data: SLUP has been tested in diet induced obese mice at doses from 25-50 mg/kg/day administered orally.
Results after chronic administration:
1)upregulation of skeletal muscle oxidative gene expression
2)upregulation of mitochondrial biogenesis markers
3)upregulation of whole-body energy expenditure
4)downregulation of fat mass
5)upregulation of treadmill endurance capacity
Effect sizes are substantial within the studies. The studies are small. The species is not human. The translation is uncertain. GRADE: Very Low
due to serious indirectness, serious imprecision, and absence of human safety data, there could be people documting their journey on it, i would use those.
The mechanism is not hard to understand. It follows predictable pathways that we can monitor if we understand them. But the absence of human pharmacokinetics means we are fucking across species without validation.
In fact, SLUP may even be a great addition to support metabolic health, so you might in the near future get it iver the counter
1)Enhances fatty acid oxidation
2)Improves insulin sensitivity
3)Promotes oxidative fiber type shift
4)Increases mitochondrial density
Results after chronic administration:
1)upregulation of skeletal muscle oxidative gene expression
2)upregulation of mitochondrial biogenesis markers
3)upregulation of whole-body energy expenditure
4)downregulation of fat mass
5)upregulation of treadmill endurance capacity
Effect sizes are substantial within the studies. The studies are small. The species is not human. The translation is uncertain. GRADE: Very Low
due to serious indirectness, serious imprecision, and absence of human safety data, there could be people documting their journey on it, i would use those.
The mechanism is not hard to understand. It follows predictable pathways that we can monitor if we understand them. But the absence of human pharmacokinetics means we are fucking across species without validation.
In fact, SLUP may even be a great addition to support metabolic health, so you might in the near future get it iver the counter
1)Enhances fatty acid oxidation
2)Improves insulin sensitivity
3)Promotes oxidative fiber type shift
4)Increases mitochondrial density
SLU-PP-332 requires chroenic administration for transcriptional effects. It works by upregulating gene expression, not by acute receptor activation.
The pharmacokinetics in humans are not reported
Rodent PK suggests oral activity with reasonable exposure. Rodents are not humans.
Human Dosage (Purely Mathematical Scaling by scientists and researchers)
mouse, 50 mg/kg:
HED = 50 × (3/37) = 4.05 mg/kg
Hypothetical equivalents:
1)60 kg female: 243 mg/day
2)90 kg male: 365 mg/day
You should only consider SLUP if you accept that the experiment is on yourself.
The pharmacokinetics in humans are not reported
Rodent PK suggests oral activity with reasonable exposure. Rodents are not humans.
Human Dosage (Purely Mathematical Scaling by scientists and researchers)
mouse, 50 mg/kg:
HED = 50 × (3/37) = 4.05 mg/kg
Hypothetical equivalents:
1)60 kg female: 243 mg/day
2)90 kg male: 365 mg/day
You should only consider SLUP if you accept that the experiment is on yourself.
Typical risks of nuclear receptor agonists in this class are metabolic, cardiac, hepatic, and oncogenic concerns. I would strictly advise against blind administration without monitoring.
Cardiac Risks:
ERRγ is highly expressed in heart tissue. upregulation of mitochondrial activity increases myocardial oxygen demand.
1)Cardiac remodeling
2)Arrhythmia risk
3)Increased myocardial oxygen demand
4)Potential for heart failure exacerbation
Metabolic Risks
1)Hypermetabolism(would consider it a pro but wtv)
2)Appetite compensation (ghrelin upregulation likely)
3)Weight rebound upon cessation, like dnp
4)Potential thyroid axis interaction
Hepatic Risks
Nuclear receptor agonists often stress liver
Unknown hepatotoxicity risk
Potential CYP induction/inhibition
Oxidative Stress:
Chronic mitochondrial upregulation may upregulate ROS
DNA damage potential
The LD50 is not reported. The NOAEL is not reported. Longterm rodent carcinogenicity studies do not exist.
Cardiac Risks:
ERRγ is highly expressed in heart tissue. upregulation of mitochondrial activity increases myocardial oxygen demand.
1)Cardiac remodeling
2)Arrhythmia risk
3)Increased myocardial oxygen demand
4)Potential for heart failure exacerbation
Metabolic Risks
1)Hypermetabolism(would consider it a pro but wtv)
2)Appetite compensation (ghrelin upregulation likely)
3)Weight rebound upon cessation, like dnp
4)Potential thyroid axis interaction
Hepatic Risks
Nuclear receptor agonists often stress liver
Unknown hepatotoxicity risk
Potential CYP induction/inhibition
Oxidative Stress:
Chronic mitochondrial upregulation may upregulate ROS
DNA damage potential
The LD50 is not reported. The NOAEL is not reported. Longterm rodent carcinogenicity studies do not exist.
| Compound | Evidence Level | Human Fat Loss | Risk Profile |
|---|---|---|---|
| Exercise | High | Moderate | Very high, tried it once, i cried. |
| Semaglutide | High | 10-15% BW | GI effects |
| GW501516 | Moderate | Small | Carcinogenic in rodents |
| SLUP | None | Unknown | Unknown |
SLUP is decades behind approved GLP1 agonists in evidence strength, it was researched in 2023, when i was still a lil jit.
i wanna use it, no conclusion tbh
1)Billon et al. — Development of synthetic ERR agonists and metabolic effects in mice
2)Rangwala et al. — ERR regulation of mitochondrial biogenesis
3)Giguère V. — ERR nuclear receptor review
3)Washington University in St. Louis group — SLU-PP-332 in diet-induced obese mice
5)Reviews on PGC-1α/ERR metabolic axis
2)Rangwala et al. — ERR regulation of mitochondrial biogenesis
3)Giguère V. — ERR nuclear receptor review
3)Washington University in St. Louis group — SLU-PP-332 in diet-induced obese mice
5)Reviews on PGC-1α/ERR metabolic axis
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